Displaying all 7 publications

  1. Muhammad HFL, Sulistyoningrum DC, Huriyati E, Lee YY, Muda WAMW
    Br J Nutr, 2021 03 28;125(6):611-617.
    PMID: 32746947 DOI: 10.1017/S0007114520003104
    The present study aimed to investigate an interaction between energy intake, physical activity and UCP2 gene variation on weight gain and adiposity changes in Indonesian adults. This is a prospective cohort study conducted in 323 healthy adults living in the city of Yogyakarta, Indonesia. Energy intake, physical activity, body weight, BMI, percentage body fat and waist:hip ratio (WHR) were measured at baseline and after 2 years while UCP2 -866G/A gene variation was determined at baseline. We reported that after 2 years subjects had a significant increment in body weight, BMI, body fat and reduction in WHR (all P < 0·05). In all subjects, total energy intake was significantly correlated with changes in body weight (β = 0·128, P = 0·023) and body fat (β = 0·123, P = 0·030). Among subjects with the GG genotype, changes in energy intake were positively correlated with changes in body weight (β = 0·232, P = 0·016) and body fat (β = 0·201, P = 0·034). These correlations were insignificant among those with AA + GA genotypes (all P > 0·05). In summary, we show that UCP2 gene variation might influence the adiposity response towards changes in energy intake. Subjects with the GG genotype of UCP2 -866G/A gene were more responsive to energy intake, thus more prone to weight gain due to overeating.
  2. Luglio HF, Sulistyoningrum DC, Huriyati E, Lee YY, Wan Muda WAM
    Nutrients, 2017 Jul 07;9(7).
    PMID: 28686191 DOI: 10.3390/nu9070716
    BACKGROUND: Obesity has been associated with leptin resistance and this might be caused by genetic factors. The aim of this study was to investigate the gene-lifestyle interaction between -866G/A UCP2 (uncoupling protein 2) gene polymorphism, dietary intake and leptin in a population based study.

    METHODS: This is a cross sectional study conducted in adults living at urban area of Yogyakarta, Indonesia. Data of adiposity, lifestyle, triglyceride, high density lipoprotein (HDL) cholesterol, leptin and UCP2 gene polymorphism were obtained in 380 men and female adults.

    RESULTS: UCP2 gene polymorphism was not significantly associated with adiposity, leptin, triglyceride, HDL cholesterol, dietary intake and physical activity (allp> 0.05). Leptin was lower in overweight subjects with AA + GA genotypes than those with GG genotype counterparts (p= 0.029). In subjects with AA + GA genotypes there was a negative correlation between leptin concentration (r= -0.324;p< 0.0001) and total energy intake and this correlation was not seen in GG genotype (r= -0.111;p= 0.188).

    CONCLUSIONS: In summary, we showed how genetic variation in -866G/A UCP2 affected individual response to leptin production. AA + GA genotype had a better leptin sensitivity shown by its response in dietary intake and body mass index (BMI) and this explained the protective effect of A allele to obesity.

  3. Muhammad HFL, Sulistyoningrum DC, Huriyati E, Lee YY, Manan Wan Muda WA
    J Nutr Metab, 2019;2019:9606054.
    PMID: 30719347 DOI: 10.1155/2019/9606054
    Background: Coffee is suggested as an alternative option for weight loss but the relationship between coffee consumption and adiposity in population-based studies is still controversial. Therefore, this study was aimed at evaluating the relationship between coffee intake and adiposity in adults and to test whether uncoupling protein 2 (UCP2) gene variation was able to affect this relationship.

    Methods: This was a cross-sectional study conducted in male and female adults living in the urban area of Yogyakarta, Indonesia. Adiposity was determined based on body weight, body mass index (BMI), percent body fat, and waist and hip circumference. Data on coffee consumption and other dietary components were collected using a semiquantitative food frequency questionnaire along with other caffeine-containing beverages such as tea, chocolate, and other beverages. The -866 G/A UCP2 gene variation was analyzed using polymerase chain reaction-restriction fragment length polymorphism. The correlation between coffee intake and adiposity was tested using linear regression test with adjustment for sex, age, energy intake, table sugar intake, and total caffeine intake.

    Results: In all subjects, coffee intake was inversely correlated with body weight (β = -0.122, p=0.028), BMI (β = -0.157, p=0.005), and body fat (β = -0.135, p=0.009). In subjects with AA + GA genotypes, coffee intake was inversely correlated with body weight (β = -0.155, p=0.027), BMI (β = -0.179, p=0.010), and body fat (β = -0.148, p=0.021). By contrast, in subjects with GG genotype, coffee intake was not correlated with body weight (β = -0.017, p=0.822), BMI (β = -0.068, p=0.377), and body fat (β = -0.047, p=0.504).

    Conclusion: We showed that coffee intake was negatively correlated with adiposity, and this was independent of total caffeine intake. Additionally, we showed that the -866 G/A UCP2 gene variation influences the relationship between coffee intake and adiposity.

  4. Oktaria V, Putri DAD, Ihyauddin Z, Julia M, Sulistyoningrum DC, Koon PB, et al.
    Arch Dis Child, 2022 Jun 09.
    PMID: 35680405 DOI: 10.1136/archdischild-2021-323765
    OBJECTIVE: To describe the prevalence and determinants of vitamin D deficiency (VDD) among healthy children aged between 0 and 18 years living in South-East Asia (SEA).

    DESIGN: We systematically searched Ovid MEDLINE and Ovid EMBASE for observational studies assessing VDD among healthy children in the SEA region as the primary or secondary outcome from database inception to 6 April 2021. PubMed was used for e-pubs and publications not indexed in Medline. Publications that included abstracts in English were included. We performed a systematic review to describe the prevalence of VDD in SEA children.

    RESULTS: Our initial search identified 550 publications with an additional 2 publications from manual screening. Of those, 21 studies from 5 different countries (Thailand, Indonesia, Vietnam, Malaysia and Cambodia) were summarised and included in forest plots. The prevalence of VDD (<50 nmol/L) ranged from 0.9% to 96.4%, with >50% of newborns having VDD, and severe VDD (<30 nmol/L) ranged from 0% to 55.8%. Female sex and urban living were the most common determinants of VDD.

    CONCLUSIONS: VDD among healthy children living in the SEA region is common. Efforts to detect VDD and the implementation of preventive measures, including education on safe sun exposure and oral vitamin D supplementation or food fortification, should be considered for key target groups, including adolescent females and pregnant and lactating women to improve the vitamin D status of newborns.

    PROTOCOL REGISTRATION NUMBER: This study is registered with PROSPERO (CRD42020181600).

  5. Samson KLI, Loh SP, Lee SS, Sulistyoningrum DC, Khor GL, Mohd Shariff ZB, et al.
    J Nutr, 2021 Aug 07;151(8):2264-2270.
    PMID: 33978167 DOI: 10.1093/jn/nxab115
    BACKGROUND: Weekly iron-folic acid (IFA) supplements are recommended for all menstruating women in countries where anemia prevalence is ≥20%; however, it is unknown whether the inclusion of folic acid in weekly IFA supplements reduces anemia.

    OBJECTIVES: We examined whether the inclusion of folic acid in weekly IFA supplements conferred any benefit on hemoglobin (Hb) concentration, anemia reduction, or iron status [ferritin and soluble transferrin receptor (sTfR)], over iron alone.

    METHODS: In this secondary analysis of a randomized controlled trial in Malaysia, n = 311 nonpregnant women (18-45 y old) received 60 mg Fe with either 0, 0.4, or 2.8 mg folic acid once-weekly for 16 wk. Fasting blood was collected at baseline and 16 wk. A generalized linear model (normal distribution with identity link) was used to assess Hb concentration at 16 wk (primary outcome).

    RESULTS: At baseline, 84% of women had low folate status (plasma folate  0.05). Baseline plasma folate concentration did not modify the effect of treatment on Hb concentration at 16 wk. Among all women, the risks of anemia [risk ratio (RR): 0.65; 95% CI: 0.45, 0.96; P = 0.03] and iron deficiency based on ferritin (RR: 0.30; 95% CI: 0.20, 0.44; P 

  6. Samson KLI, Loh SP, Khor GL, Mohd Shariff Z, Yelland LN, Leemaqz S, et al.
    BMJ Open, 2020 02 05;10(2):e034598.
    PMID: 32029499 DOI: 10.1136/bmjopen-2019-034598
    INTRODUCTION: Folic acid (0.4 mg) taken prior to and during early pregnancy reduces the risk of neural tube defects (NTDs). Because these birth defects occur early in pregnancy, before women may know they are pregnant, many countries have mandated the addition of folic acid to food staples. In countries where fortification is not possible, and weekly iron folic acid programmes exist to reduce anaemia, the WHO recommends that 2.8 mg (7×0.4 mg) folic acid be given instead of the current weekly practice of 0.4 mg. Currently, there is a lack of evidence to support if the 2.8 mg folic acid per week dose is sufficient to raise erythrocyte folate concentrations to a level associated with a reduced risk of a NTD-affected pregnancy. We aim to conduct a three-arm randomised controlled trial to determine the effect of weekly folic acid with iron on erythrocyte folate, a biomarker of NTD risk.

    METHODS AND ANALYSIS: We will recruit non-pregnant women (n=300; 18-45 years) from Selangor, Malaysia. Women will be randomised to receive either 2.8, 0.4 or 0.0 (placebo) mg folic acid with 60 mg iron weekly for 16 weeks, followed by a 4-week washout period. The primary outcome will be erythrocyte folate concentration at 16 weeks and the mean concentration will be compared between randomised treatment groups (intention-to-treat) using a linear regression model adjusting for the baseline measure.

    ETHICS AND DISSEMINATION: Ethical approval was obtained from the University of British Columbia (H18-00768) and Universiti Putra Malaysia (JKEUPM-2018-255). The results of this trial will be presented at scientific conferences and published in peer-reviewed journals.

    TRIAL REGISTRATION NUMBERS: ACTRN12619000818134 and NMRR-19-119-45736.

  7. Samson KLI, Loh SP, Lee SS, Sulistyoningrum DC, Khor GL, Shariff ZBM, et al.
    BMJ Glob Health, 2020 12;5(12).
    PMID: 33272946 DOI: 10.1136/bmjgh-2020-003897
    INTRODUCTION: Weekly iron-folic acid (IFA) supplements are recommended for all menstruating women in countries where anaemia prevalence is >20%. Anaemia caused by folate deficiency is low worldwide, and the need to include folic acid is in question. Including folic acid might reduce the risk of a neural tube defect (NTD) should a woman become pregnant. Most weekly supplements contain 0.4 mg folic acid; however, WHO recommends 2.8 mg because it is seven times the daily dose effective in reducing NTDs. There is a reluctance to switch to supplements containing 2.8 mg of folic acid because of a lack of evidence that this dose would prevent NTDs. Our aim was to investigate the effect of two doses of folic acid, compared with placebo, on red blood cell (RBC) folate, a biomarker of NTD risk.

    METHODS: We conducted a three-arm double-blind efficacy trial in Malaysia. Non-pregnant women (n=331) were randomised to receive 60 mg iron and either 0, 0.4, or 2.8 mg folic acid once weekly for 16 weeks.

    RESULTS: At 16 weeks, women receiving 0.4 mg and 2.8 mg folic acid per week had a higher mean RBC folate than those receiving 0 mg (mean difference (95% CI) 84 (54 to 113) and 355 (316 to 394) nmol/L, respectively). Women receiving 2.8 mg folic acid had a 271 (234 to 309) nmol/L greater mean RBC folate than those receiving 0.4 mg. Moreover, women in the 2.8 mg group were seven times (RR 7.3, 95% CI 3.9 to 13.7; p<0.0001) more likely to achieve an RBC folate >748 nmol/L, a concentration associated with a low risk of NTD, compared with the 0.4 mg group.

    CONCLUSION: Weekly IFA supplements containing 2.8 mg folic acid increases RBC folate more than those containing 0.4 mg. Increased availability and access to the 2.8 mg formulation is needed.

    TRAIL REGISTRATION NUMBER: This trial is registered with the Australian New Zealand Clinical Trial Registry (ACTRN12619000818134).

Related Terms
Contact Us

Please provide feedback to Administrator (afdal@afpm.org.my)

External Links